Alzheimer’s disease (AD) still prevails and continues to increase indiscriminately throughout the 21st century, and is thus responsible for the depreciating quality of health and associated sectors. AD is a progressive neurodegenerative disorder marked by a significant amassment of beta-amyloid plaques and neurofibrillary tangles near the hippocampus, leading to the consequent loss of cognitive abilities. Conventionally, amyloid and tau hypotheses have been established as the most prominent in providing detailed insight into the disease pathogenesis and revealing the associative biomarkers intricately involved in AD progression. Nanotheranostic deliberates rational thought toward designing efficacious nanosystems and strategic endeavors for AD diagnosis and therapeutic implications. The exceeding advancements in this field enable the scientific community to envisage and conceptualize pharmacokinetic monitoring of the drug, sustained and targeted drug delivery responses, fabrication of anti-amyloid therapeutics, and enhanced accumulation of the targeted drug across the blood–brain barrier (BBB), thus giving an optimistic approach towards personalized and precision medicine. Current methods idealized on the design and bioengineering of an array of nanoparticulate systems offer higher affinity towards neurocapillary endothelial cells and the BBB. They have recently attracted intriguing attention to the early diagnostic and therapeutic measures taken to manage the progression of the disease. In this article, we tend to furnish a comprehensive outlook, the detailed mechanism of conventional AD pathogenesis, and new findings. We also summarize the shortcomings in diagnostic, prognostic, and therapeutic approaches undertaken to alleviate AD, thus providing a unique window towards nanotheranostic advancements without disregarding potential drawbacks, side effects, and safety concerns.

Fungal ribosomally synthesized and post-translationally modified peptides (F-RiPPs) embody a paradoxical duality, transitioning from lethal mycotoxins to precision oncology payloads via antibody-drug conjugates (ADCs). This review portrays the biosynthetic logic of canonical families - amatoxins/phallotoxins, dikaritins, epichloëcyclins, and emergent asperigimycins, emphasizing PTMs like macrocyclization, N-methylation, and oxidative cross-links that confer proteolytic stability, membrane permeability, and target affinity. Genome mining pipelines integrating antiSMASH, seq2ripp, HypoRiPPAtlas, and GNPS molecular networking accelerate cryptic BGC decryption, heterologous expression in yeast/filamentous fungi, and combinatorial refactoring for analog libraries. Pharmacologically, F-RiPPs inhibit RNA Pol II (amatoxins), disrupt microtubules (dikaritins), perturb membranes (borosins), and induce lipid-mediated apoptosis (asperigimycins), with preclinical IC50s of 1–50 nM/μM and therapeutic indices >100 in xenografts. Translational exemplars include Heidelberg Pharma's ATACs, achieving Phase I/IIa remissions in myeloma/NHL via BCMA/CD37-targeted amanitin delivery. Addressing bottlenecks in silent cluster activation, enzyme mechanistics, and GMP-scaleup, a roadmap proposes ML-driven prioritization and automated heterologous platforms to harness untapped RiPP diversity for MDR-evasive, bystander-active therapeutics.